REPERFUSION INJURY AND LIPID ABSORPTION

临床和实验都已证明， 随后再灌注（I/R）对胃肠道是有害的。 然而，大多数研究集中在微血管或大体上， 粘膜的形态学变化。 上皮细胞膜的变化 对大分子的渗透性也被用于评估粘膜的渗透性。 损伤，但该指数提供的关于功能的信息很少 肠粘膜的完整性。 初步数据表明 肠脂质吸收对I/R诱导的损伤敏感， 因此，它可能是一个有用的肠粘膜功能指标 I/R侮辱后的完整性。 因此，我们假设：（1）I/R的 小肠导致其吸收和运输A的能力降低， 试餐血脂的降低与缺血持续时间有关; (2)肠脂质吸收是一个有用的粘膜功能指标 完整性;（3）恢复正常的肠道脂质吸收， 在肠上皮细胞增殖和随后的替换之前， 受损细胞的健康肠上皮细胞;和（4）鸟氨酸脱羧酶是 参与修复过程。 为了验证这些假设，我们将 以下实验： 具体目标1：通过研究 I/R对A消化、吸收和淋巴转运的影响 含有甘油三酯和胆固醇的血脂测试餐。 具体目标2：确定小肠损伤的程度， 在I/R侮辱之后的不同时间。 具体目标3：评估鸟氨酸脱羧酶参与 I/R损伤肠的修复。 具体目标4：研究I/R后肠粘膜的修复- 诱导损伤。 具体目标5：研究饮食与易感性的关系 小肠的I/R诱导损伤。 建议的研究将大大提高我们对这些因素的认识 影响I/R引起的损伤以及损伤如何反过来影响 小肠的功能。 这项研究还将提供新的和 有用的信息有关的过程中所涉及的修复的小 肠I/R诱导损伤后。 因此，本报告提供的信息 研究不仅与肠粘膜损伤有关， 肠道移植

It has been demonstrated both clinically and experimentally that ischemia followed by reperfusion (I/R) is injurious to the gastrointestinal tract. However, most studies have focused either on the microvasculature or gross morphological changes in the mucosa. Changes in epithelial membrane permeability to macromolecules have also been used to assess mucosal damage, but this index provides little information regarding the functional integrity of the intestinal mucosa. Preliminary data indicate that intestinal lipid absorption is sensitive to I/R-induced injury and therefore it may be a useful functional index of intestinal mucosal integrity after I/R insult. We therefore hypothesize that: (1) I/R of the small bowel results in a reduction of its ability to absorb and transport a lipid test meal and the reduction is related to the duration of ischemia; (2) intestinal lipid absorption is a useful functional index of mucosal integrity; (3) restoration of normal intestinal lipid absorption is preceded by the proliferation of enterocytes and the subsequent replacement of injured cells by healthy enterocytes; and (4) ornithine decarboxylase is involved in the repair process. To test these hypotheses, we will perform the following experiments: Specific Aim 1: Establish and characterize our model by studying the effect of I/R on the digestion, absorption and lymphatic transport of a lipid test meal containing triglyceride and cholesterol. Specific Aim 2: Determine the extent of injury to the small intestine at various times following the I/R insult. Specific Aim 3: Assess the involvement of ornithine decarboxylase in the repair of the intestine injured by I/R. Specific Aim 4: Study the repair of the intestinal mucosa after I/R- induced injury. Specific Aim 5: Study the relationship between diet and the susceptibility of the small intestine to I/R-induced injury. The proposed studies will greatly enhance our understanding of the factors affecting I/R-induced injury and how the injury in turn affects the function of the small intestine. This study will also provide new and useful information regarding processes involved in the repair of the small intestine after I/R-induced injury. Thus the information provided by this study will not only be relevant to intestinal mucosal injury but also to intestinal transplants.